Repeated injections of cholecystokinin (CCK) during a period of up to 3 weeks significantly increased the weight of the pancreas in rats. This was associated with an increase in the amount of protein per unit weight of DNA, suggesting hypertrophy of the acinar cells, and with increase in the total amount of pancreatic DNA, indicating additional hyperplasia of the gland. CCK administration also increased the pancreatic content of amylase and trypsin, but the content of lipase remained unchanged. The rate of secretion of the two enzymes increased in the CCK-treated rats, although it appeared that the functional capacity of the individual pancreatic acinar cells was not increased. CCK injections had no effect on the insulin content of the pancreas or on the composition of the partoid glands. Repeated injections of secretin in the doses used in this study had no effect on the pancreas.
The S3-guidelines contain evidence-based recommendations for the indication, selection of procedure, technique, and follow-up. Patient care should improve after implementation of these guidelines in clinical practice. Compliance by decision makers and health insurers is warranted.
SUMMARY Because somatostatin (SRIF) reduces exocrine pancreatic secretion, its effect on acute pancreatitis was investigated in rats. Linear SRIF reduced serum amylase and lipase but had no effect on pancreatic necrosis, oedema, leucocyte infiltration, and enzyme content. The mortality rate was not reduced. These results do not recommend the use of SRIF in the treatment of acute pancreatitis.Cyclic somatostatin (SRIF) significantly reduces hormonal Dollinger et al., 1976;Domschke et al., 1976) and non-hormonal stimulated pancreatic volume and enzyme secretion in man. Linear SRIF inhibits basal and hormonal stimulated enzyme secretion in the rat (Folsch et al., 1976). As 'rest to the gland' is generally considered to be a major aim in the treatment of acute pancreatitis (Trapnell, 1972) the effect of SRIF was investigated in acute experimental pancreatitis in the rat.
MethodsAcute experimental pancreatitis was induced by retrograde injection of 0-6 ml of 0-8, 2-0, 2-5, and 3-0 Na-taurocholate (Serva Feinbiochemica, Heidelberg) into the pancreatic ducts of 101 male Wistar rats (180-220 g) (Lankisch et al., 1974). Linear SRIF (Serono, Freiburg) was given subcutaneously at a dosage of 200 ,ug during operation as a bolus injection followed by infusion of 100 ,ug/100 g body weight/h for three hours. This regime had been found to decrease significantly pancreatic enzyme secretion for more than four hours (Folsch et al., 1976). Controls received saline infusions. To investigate the SRIF influence upon the survival rate the following groups were formed (Figure) : (a) SRIFtherapy: n = 6; (b) controls: n = 5; 0-8 %-Na-taurocholate-pancreatitis was not used for survival experiments as the mortality rate of this model is too low to demonstrate the success of a treatment.To study the effects of SRIF upon morphological and enzymatic factors rats were killed four hours after induction of pancreatitis by 0-8, 2-0, and 3 0%-Na-taurocholate-that is, one hour after the treatment was stopped. 2 5%-Na-taurocholate-pancreatitis was not used as there were no distinct differences between 2-0 and 3 0 %-Na-taurocholate-pancreatitis where the above mentioned factors were concerned (Table). Ascites was measured and tissue from the head and the tail of the pancreas was fixed in Bouin's solution, embedded in paraffin, cut in 5 ,um sections, and stained with haematoxylin and eosin.
Indomethacin given orally or intramuscularly before or shortly after induction of acute sodium-taurocholate or olive-oil-induced pancreatitis in rats reduced the lethality. Neither the enzyme content of serum, ascites, and pancreatic tissue nor the damage to the organ itself were changed under the influence of indomethacin. Thus a modification of systemic effects of acute pancreatitis may be responsible for the beneficial effect of indomethacin.
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